Ventilator - Associated Pneumonia (VAP)

BR Bansode

INTRODUCTION

VAP is subtype of hospital acquired pneumonia which 5 days. But it is very high i.e. 70% in pts who ventilated for
occur in people who are on mechanical ventilator, through 30 days. Once pts is off the ventilator & transfer to ward/
endotracheal tube (ET) or tracheotomy tube for at least home the incidence of VAP drops significantly in the absence
48 hrs. VAP is medical condition that result from infection of other risk factors for pneumonia.
which floods the alveoli - small, air-filled sacs in the lung
responsible absorbing oxygen from atmosphere. ETIOLOGY OF VAP
MDR non MDR pathogens are potential agent causing VAP.
VAP is distinguished from other type of pneumonia (HAP, Non MDR pathogens are identical to pathogen found in
CAP) by different types of microorganism (MDR, non MDR) severe CAP. The VAP develop in first 5-7 days of mechanical
responsible, use of antibiotics, methods of diagnosis, ventilation.
ultimate prognosis & effective preventive measures.
In patients having other risk factors for HCAP, MDR pathogen
EPIDEMIOLOGY may vary from hospital to hospital & different critical care
VAP is common complication amongst patients who require unit in same institution. Many hospital have problem with
mechanical ventilations. Prevalence is 6-52 cases per 100 pts P. aeruginosa & MRSA. Viral & fungal infection causing VAP
on any given day in ICU an average of 10% of pts will have is less common, but in immunocompramised pts VAP can
VAP. The frequency of diagnosis is not static but changes cause by these organism. (Table I).
with duration of mechanical ventilation, but highest in first
Table I. Microbiologic Causes of Ventilator- Associated Pneumonia

Non - MDR Pathogens MDR Pathogens

Streptococcus pneumoniae Pseudomonas aeruginosa
Other streptococcus SPP. MRSA
Haemophilius influenzae Acinetobacter SPP.
MSSA Antibiotic- resistant Enterobacteriaceae
Antibiotic - sensitive Enterobacteriaceae Enterobacter SPP.
Escherichia Coli ESBL - positive strains
Klebsiella pneumoniae Klebsiella SPP.
Proteus SPP. Legionella pneumophila
Enterobacter SPP. Burkholderia cepacia
Serratia marcescens Aspergilius SPP
ESBL, extended -spectrum β lacttamase; MDR, mutidrug - resistant;
MRSA, methicillin - resistant Staphylococcus aureus; MSSA, methicillin -sensitive S. Aureus.
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Pathology respiratory tract.

The three factors are critical in pathogenesis of VAP 3. Compromise of the normal host defense mechanism.
1. Colonization of the oropharynx with pathogenic (Table II)
microorganism, The most obvious risk factor is ET, which by pass the
2. Aspiration of these pathogen from oropharynx into lower normal mechanical factors preventing aspirations. But
Table II. Pathogenic mechanisms and corresponding prevention strategies for ventilator associated pneumonia
Pathogenic Mechanism Prevention strategy

Oropharyngeal colonization with

pathogenic bacteria
Elimination of normal flora Avoidance of prolonged
antibiotic courses

Large-volume oropharyngeal Short course of prophylactic

aspiration around time antibiotics for comatose patients
of intubation

Gastroesophageal reflux Postpyloric enteral feeding,

avoidance of high gastric residuals,
prokinetic agents

Bacterial overgrowth of stomach Avoidance of gastrointestinal bleeding

due to prophylactic agents that raise gastric PH,
selective decontamination of digestive tract with
nonabsorbable antibiotics

Cross-infection from other Hand washing, especially with alcohol-

colonized patients based hand rub; intensive infection control
education; isolation; proper cleaning of
reusable equipment

Large -volume aspiration Endotracheal intubation; avoidance of

sedation; decompression of small-bowel

obstruction
Microaspiration around
endotracheal tube
Endotracheal intubation Noninvasive ventilation
Prolonged duration of Daily awakening from sedation
ventilation weaning protocols

Abnormal swallowing function Early percutaneous tracheostomy

Secretions pooled above Head of bed elevated; continuous

endotracheal tube aspiration of subglottic secretions
with specialized endotracheal
tube; avoidance of reintubation;
minimization of sedation and patient transport

Altered lower respiratory host defenses Tight glycemic control; lowering of

hemoglobin transfusion threshold; specialized
enteral feeding formula
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microaspiration can reach lower respiratory tract. ET & tract require 103 cfu/ml the sample from lower resp. tract
suctioning can damage the tracheal mucosa, facilitating should be collected properly by bronchoscopy or BAL to
tracheal colonization. Pathogenic bacteria can form a increase sensitivity. The IDSA & ATS guideline have suggested
glycocalyx biofilin on ET surface that protect them from that all these methods are appropriate & choice depends
antibiotic & host defenses. These pathogen can dislodged on availability & local expertise. High diagnostic threshold
during suctioning & small fragement of glucolyx can embolise can be obtained if sample taken before starting of antibiotic
to lower respiratory tract carrying bacteria with them. therapy or changed the antibiotic.

In critically ill pts normal oropharyngeal flora replaced by The clinical approach (CPIS) improve the diagnostic criteria.
pathogenic microorganism, cross infection from other pts The clinical pulmonary infection score was developed
or paramedicals, contaminated equipment & malnutrition considering various clinical criteria. The CPIS can help to
contribute to development of VAP. Severely ill pts with sepsis decide the choice antibiotic requirement, MDR coverage to
& trauma enter a state of immunoparalaysis several days be given or not and outcome of VAP affected individuals.
after admission in ICU are greater risk of developing VAP. (Table III).
Hyperglycemia affect neutrophil function & many recent
trial have shown that keeping blood sugar close to normal Transport of bacteria from sinus, stomach or blood stream
with exogenous insulin have beneficial effects like decrease is rare.
risk of infection. The frequent blood transfusion (leukocyte
depleted) also affect the immune response in individual pts. CLINICAL MANIFESTATION
The clinical manifestation of VAP in pts who are on
The quantitative culture approach is to discriminate between mechanical ventilation are often sedated & are unable to
colonization and true infection. The sampling from lower communicate. Many typical presentation of pneumonia
respiratory tract exclude the colonization & require lower will be either absent or unable to be obtained. The most
threshold of growth necessary to diagnose pneumonia. For important S/S are fever or low body temperature new
example samples endotracheal aspirate require diagnostic purulent sputum, hypoxia, leukocytosis, appearance of
threshold is 106 cfu/ml the sample from lower respiratory new infiltrate on x-ray chest or consolidation, other signs
like tachypnea, tachycardia, increase minute ventilation.
Table III. Clinical Pulmonary Infection Score (CPIS)
DIAGNOSIS
VAP should be suspected in any patients on mechanical
ventilation exhibiting increasing leukocyte count, new
shadows (infiltrate) on chest x-ray as is indicative of
pneumonia. Blood culture may reveal the microorganism
causing VAP. The strategic approach i.e. collect culture from
trachea/ET & new or enlarging infiltrate on x-ray chest. The
other is invasive i.e. bronchoscopy plus bronchoalveloar
lavage for pts with evidence of VAP. When both these
methods yield negative culture the diagnosis of VAP is
unlikely.

The differential diagnosis of VAP is a typical pulmonary

edema, pulmonary contusion/hemorrhage, hypersensitivity
pneumonia, ARDS & pulmonary embolism. Clinical finding
inventilated patient with fever & leukocytosis may have
different diagnosis than VAP, like antibiotic associated
@ The progression of the infiltrate is not known and tracheal diarrhea, sinusitis, UTI, pancreatitis, drug fever, which
aspirate culture results are often unavailable at the time of require antibiotic from different group than VAP, surgical
the original diagnosis; thus, the maximal score is initially 8-10
Note: ARDS, acute respiratory distress syndrome; CHF, drainage, or catheter removal for optimal management.
congestive heart failure
418 Medicine Update-2011

MANAGEMENT OF VAP Once etiologic diagnosis is made the antibiotic therapy may
Management of VAP should be matched to known causative be with single drug in 50% cases, while in 25% pts require
bacteria. When first time VAP is suspected bacteria causing two drug combination, like ? lactum & aminoglycosides.
infection is typically not known then broad spectrum VAP causes by MRSA is associated with 40% clinical failure,
antibiotic (Empiric therapy) are given until particular Linezolid is more efficacious than standard dose of
bacterial culture and sensitivity determined. Empiric vancomycin in pts with renal insufficiency.
therapy should be started taking into both risk factors
particular resistance bacteria as well as local prevalence of FAILURE TO IMPROVE
resistance microorganism. So management entirely depends Treatment failure is more common in VAP caused by MDR
on knowledge of local flora which vary from hospital to pathogen. 40% failure when VAP (MRSA) treated with
hospital. (Table IV). vancomycin & 50% failure in VAP caused by P.aeruginosa by
any antibiotics.
If MDR pathogen not suspected the VAP should be
treated with antibiotic used for severe CAP. However MDR Recurrent VAP caused by same pathogen is possible because
pathogen isolated like drug resistance MRS & ESBL positive of biofilim on ET allows reintroduction of microorganism. VAP
Enterobacteriaceae or intrinsically resistant pathogen P due to new super infection and pressure of extra pulmonary
aeruginosa & acinetobacter, the β lactum drug specially infection & drug toxicity must be consider in the differential
cephalosporin should be given. P aeruginosa develop diagnosis of treatment failure.
resistance to all routinely used antibiotics. Acinctobacter,
stenotrophomanas maltophillia & Burkholderia cepacia are COMPLICATIONS
intrinsically resistance to many empiric antibiotic regimens Apart from death, the major complication of VAP is
or during therapy of VAP. prolongation of mechanical ventilation & stay in ICU. Some
time necrotizing pneumonia & pulmonary hemorrhage occur
Most pts without risk factor for MDR infection should due to pseudomonas aeruginosa. Bronchiectasis & pulmonary
be treated with single agent. Legionella which can be scarring leading to recurrent pneumonias, catabolic state in
nosocomial microorganism in VAP, where potable water pts who is malnourished. Elderly pts more crippled & need
deficiency in the hospital. lifelong nursing care.

Table IV. Empirical Antibiotic Treatment of Health Care - Associated Pneumonia

Patients without Risk factors for MDR Pathogens

Cefriaxone (2g IV q24h) or
Moxifloxacin (400mg IV q24h), Ciprofloxacin (400mg IV q8h), or Levofloxacon
(750mg IV q24h) or
Ampicillin/ sulbactam (3g IV q6h) or
Ertapenem (1g IV q24h)

Patients with Risk Factors for MDR Pathogens

1. A β- lactam
Ceftazidime (2g IV q8h) or Cefepime (2g IV q8 - 12h) or
Piperacillin/tazobactam (4.5 g IV q6h), imipenem (500mg IV q6h or 1 g IV q8h), or meropnem (1g IV q8h) plus
2. A second agent active against gram - negative bacterial pathogens:
Gentamycin or tobramycin (7 mg/kg IV q24h) or amikacin (20mg/kg IV q24h) or
Ciprofloxacin (400mg IV q8h) or levofloxacin (750 mg IV q24h) plus
3. An agent active against gram - positive bacterial pathogens:
Linezolid (600mg IV q12h) or
Vancomycin (15mg/kg, up to 1 g IV, q12h)
MDR, multidrug-resistant
 Medicine Update-2011 419

The clinical improvement if it occur is evident in first 48 to72 nasal or face mask can avoid ET associated risk factors.
hrs of initiation of antibiotic therapy. Hypoxia disappear but  Early extubation, avoiding heavy sedation, proper aseptic
clinical infiltrate initially worsen during the treatment, the precaution for suction procedure, use of mouth wash can
clinical criteria are good indicator of response to therapy in reduced incidence of VAP.
VAP. Once pts is improved stable follow up with x-ray chest  Reintubation, transport pts for different procedure have
may not be necessary for few weeks. higher incidence of VAP. Recently use of silver coating
ET may also reduce incidence of VAP.
PROGNOSIS  Elevating head end 30-45° above horizontal significantly
VAP is associated with 50-70% mortality. Pts who develop VAP reduce VAP rate.
are at least twice risk of death than who do not develop.  MRSA & the nonfermenters P.aeruginosa & Acinetobacter
SPP are normally not part of bowel flora but resides
VAP in trauma pts mortality is less. VAP caused by MDR primarily in the nose & on the skin respectively. So
pathogen has significant mortality than non MDR pathogen. controlling overgrowth of bowel flora & proper cleaning
VAP caused by S.Maltophilia is a marker for pts who is of nose & skin can reduce VAP rate.
immunocompramised that death is inevitable.  Consistant infection control practice in hospital/ICU can
minimize VAP rate.
PREVENTION
 At early stages of illness use of noninvasive ventilation via

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